Tag Archives: research

There’s a lot to think about if you’re considering being part of a clinical trial.

Some trials are more risky than others. These two are probably less risky, but you still need to ask:

What are the potential risks?

How many people/ what percentage have these risks

What are the potential side-effects?

How many people /what percentage get these?

What can be done if I do have a side effect or risk? Is it reversible?

What are the potential benefits?

What percentage have had these benefits?

How much of these had similar condition at a similar stage to me?

How long do they last?

Is more treatment necessary?

How much does it cost?

Will you give information either to me or to my doctor about what therapy I have undergone?

How will I be monitored? Eg scans, bloodtests etc

How often will I have to return for follow up? Is there a charge?

Will they pay my travel expenses?

How will I know if it’s worked? What’s the timescale for improvement?

Is there a placebo ( dummy drug) group? If I’m in the placebo group, and the real treatment group benefit, will I have the chance to change to the treatment group?

If I have the treatment during the trial, and benefit from it, will I be able to carry on with it long term?

Biotin

I’ve posted before about biotin in MS. A medical preparation of it has been given the name MD1003, and it is now being trialled to see its effect on people with progressive MS. If you’re interested, here are the contacts. Don’t forget to ask those questions!

Statins

My personal suspicion is that the beneficial effects are from lowering the bad fats in the blood, and that a safer and more healthy way to do this would be to adjust lifestyle factors; primarily diet, along the lines of the advice at http://www.overcomingms.org…. However, there may be some other mode of action, or radical lifestyle change may not be possible for you, in which case, you can register your interest for the trials, so that somebody will contact you when they start recruiting, which should be very soon ( summer of 2017), here:

Consensus was: safety is improving – from 2011 the mortality rate has been 0.3% rather than 1-2%. Due to impressive rates of NEDA ( no evidence of disease activity – relapses or on MRI) – 80% at 2 years and 70% at 4 years in one study;

Yes, but ONLY in cases of early/new, highly active/aggressive relapsing remitting MS, where person is young, still walking, and treatment with first & second line treatment have failed.

And now for something completely different, and please DO try this at home(!): Seriously, I will be

This beautifully carried out RCT had people with progressive forms of MS taking 1,200mg of Lipoic Acid, a supplement often sold as an ‘anti-oxidant’, and also called ‘alpha-lipoic acid’ once a day. A control group took a placebo.

After 2 years, the group taking the lipoic acid had a whopping 66% less brain atrophy on MRI scan ( showing less loss of brain cells), taking them back to a normal rate of brain atrophy, and half the number of falls.

Love it when something so harmless is investigated properly and found effective. Especially good to have something positive for progressive MS!

showed that as we know, effectiveness in reducing relapses from lowest up goes: Interferons, then Fingolimod, then Alemtuzemab and Tysabri. The last 2 showed the same effectiveness in preventing relapses. Natalizumab also showed improvement in disability in the first year, but not after that. and as we now the side effect profile and the way you take it is very different. Tysabri also has a rebound effect if and when you stop taking it.

Alemtuzemab

research was presented that showed this drug performing very well in ‘resetting’ the immune system. Around 60% of people did not need more than 2 infusions, and NEDA ( no evidence of disease activity) was very high., but only when used EARLY. Time to change from the ‘wait and see’ attitude? This is the push from leading MS experts. Maybe check in with the MS Brain Health campaign if your neurologist is dragging their feet.

Vitamin D

very strong evidence coming through from numerous sources that notwithstanding previous medical controversies and uncertainties, all people with MS should be on high dose from diagnosis – 4-5000 IU daily at least, and testing ( backs up info already posted on this blog) MS Base ( a database with over 41,000 people with MS’s records) showed a clear seasonal peak in relapses around the world, at the end of winter; with a time lag, shorter in colder countries. Low vitamin D levels were the strongest risk for progression in another study, and added a further anti inflammatory effect to people already on a disease modifying treatment, in another.

One study found that people with MS given 100,000 twice a month for 2 years had a 60% reduction in relapse rate, and a 78% reduction in new lesions, compared to placebo. Powerful stuff, hopefully enough to finally swing the doubters.

Siponimod for progressive MS

presented as promising new treatment but I missed that session so – investigate!

Scientific highlights presentation – was split into 3 sections ‘migration and CNS injury’, ‘Gut and Food’ and ‘remyelination and oligodendracytes’

At the end of the event, I was really surprised to see these slides in the highlights – I missed the full presentation but one slide went like this:

Went on to describe how animals with this experimental model of MS respond very well to hyperbaric oxygen: Oxygen therapy reduces pattern 3 demyelination.

So maybe we will see some new research showing usefulness of hyperbaric oxygen? If you can access it, I always say that it’s worth trying, and observe the effects on yourself.

Diet and Gut in MS

Feels like finally, the importance of aspects of diet is being addressed and listened to in MS research. In fact all present were enjoined Not to ignore environmental factors. Hurrah! a strike for logical thinking!

This was a feature of quite a lot of research at ECTRIMS. Lots of research on the role of the Biome ( bacteria in the gut) and how it affects MS. Interesting, exciting, but we still haven’t nailed practical application yet, so best bet is Take a daily probiotic capsule or powder, with as many different strains in as possible. And do these things, discussed previously.

Being overweight was identified as a serious risk factor for both developing, and worsening with MS. If you’ve got pounds to lose, check out the excellent ‘Fast Diet/ 5:2 diet’, showcased by Micheal Moseley on the BBC -https://thefastdiet.co.uk/ fasting also has benefits for inflammatory conditions.

Salt:

salt stored in the skin was posed as a driver for auto-immune neuroinflammation in one paper. People with MS were found to have higher levels of salt in the skin….so that too… we could all cut down our salt – most is found in processed foods… and as you do it, your tastebuds acclimatise so it won’t mean you won’t taste your food.

Ending on a high

Conference ended on a high note, celebrating the huge progress that has been made in preventing disability – progress that started even before the availability of the disease modifying drugs, but has in recent years added a further 15 years of non-disabled life to the average MS-er, and is still making leaps and bounds.

I hope I’ve made an accurate summary of the sessions that I attended – mistakes are possible, and they will be all mine. If you spot one, please let me know!

Hello from the 32nd congress of ECTRIMS, & the 21st conference of Rehabilitation in MS.

ECTRIMS is ‘ Europe’s and the world’s largest professional organisation dedicated to the understanding and treatment of multiple scelrosis’

With over 8000 delegates, all specialising, of with a special interest, in MS, it’s a privilege to attend! Loads of lectures run concurrently, so you can never attend everything. And the really science-y lectures, that are not yet going to make a practical difference to my patients, tend to go over my head a bit. Or a lot, depending! So here’s a digest of what I’ve learned so far, that has a practical application for people with MS!

The intro – X. Montalban (Spain)

Good to hear the current aims:

Evolving the Diagnosis of MS, so it can be made more quickly, but still be accurate. ( did you know there are 100 other conditions that can cause MS -like symptoms?)

getting better at Prognosis – working out who is likely to develop definite MS, and who with MS is most at risk of becoming disabled

in order to Personalise treatment – this means ” the right drug, at the right time, for the right person. And, at the right price.” Moving away from ‘first-line’ and ‘second-line’ treatments, to personalised treatments. Did you know that people treated with a disease modifying treatment before the second relapse developed less disability?

This leads into a presentation I saw in the break:

Brain Health – G. Giovanonni (UK)

This is a campaign led by Gavin Giovanonni of Bart’s ( UCL) hospital, London, and an international steering group of MS experts, with funding from some of the major disease modifying therapy (DMT) manufacturers.

The focus was on healthcare professionals, to improve services for people with MS, with, again, speedier diagnosis, prompt treatment, adequate follow up to find out if treatment is working, to allow an alternative or more aggressive treatment if the original one is not having a good enough effect, and certain standards of MS care – eg – noone with MS should get a pressure sore in your area of care etc.

People with MS can get involved with this project, and download the guide to help get what you need from your neuro services. It also strongly recommends the lifestyle measures to keep your brain healthy that have the most robust clinical evidence in MS to satisfy the health service, like:

This presentation was kind of frustrating. Only because we all know physios, OTs, psychologists, physical therapists who do great work that makes a big difference to people with MS’s health and lives. But because we’re not organised or funded to perform large scale randomised controlled trials ( as drugs are), most of the studies done aren’t ‘robust’ enough to prove the effects. This is a problem in and with the evidence based medicine approach – it has a tendency to turn all medicine into pharmaceutical medicine.

The interventions whose evidence is robust enough are:

Exercise ( this is coming up time and time again! Did you know that exercise has recently been found to be not just good for you in all the ways we already know, but actively anti-inflammatory?)

Endurance training, and

Supported treadmill walking ( probably not massively better than other interventions, just done good research, possibly due to industry funding)

Improving mobility – D. Centonze ( Italy)

An extremely scientific presentation, suggesting that mobility could be preserved by measures that help to restore excitability to the nerve connections; ‘long term potentation’ and ‘synaptic plasticity’

At this point I really wished that the organisers would round up their presenters and give them presentation skills; however, what I THINK he said was:

Certain interventions can restore excitability, and thus improve mobility. And these are:

Exercise ( yes, exercise again!)

SSRI antidepressants (I’d have to know a lot more about that before recommending this. Like, is this all theoretical or have they conducted studies to show this effect??

Now this was really interesting. Why people get such fatigue in MS has always been a big question, and one that there are a lot of theories about. These investigators wanted to see
whether it was more associated with damage and lesion load in the brain, which can be measured by MRI scanning, or by inflammation, which can be measured by inflammatory markers in the cerebrospinal fluid ( CSF ) taken by lumbar puncture.

What they found, was that there was no significant relationship between damage and lesion load in the brain, but there was a significant relationship between inflammatory markers in the CSF. This suggests that inflammation, rather than structural damage, is responsible for fatigue in MS.

The take-home from this is that there are many ways to help reduce inflammation in your body – both your drug treatment, and lifestyle measures – eating an anti-inflammatory diet, getting good rest and sleep, becoming more resilient to stress, exercising, sunshine, vitamin D…

Dual lead deep brain stimulation for tremor – S. Oliveria (USA)

Study showing good effects on refractory ( ie won’t respond to any treatment/ drugs) tremor, in a small group of 11 people. 8 (73%) showed benefit at 6 months. 2 did not benefit; they had ataxia ( like clumsiness) rather than tremor. One got infected and had to have the leads removed. Kind of let down by the fact that they used a scale to show effectiveness, which didn’t show the actual result for the person’s functional improvement. So worth finding out about, but not a sure thing until we hear what the results of treatment for the actual people were. Grr!

How come other auto-immune diseases get articles like this in medical journals??

Even though this is about rheumatoid arthritis, it’s well worth reading if you have MS.

It confirms many things I’ve said here before. It is technical, and hard going but – scan it, and get the gist. For me, the low sat. fat diet is a cornerstone in MS, as per http://www.overcomingms.org. but I’m getting to think that individual intolerances can be wreaking havoc in some people, too. You read a lot of good discussions like this in natural health experts, but never in the medical literature for MS.

In spite of the great advances that have been made in the development of new drugs for the treatment of rheumatoid arthritis (RA), many patients are interested in alternative treatments like dietary therapy. Although relatively few studies have been carried out on the possible impact of dietary therapy on disease activity in RA, interest in this matter is growing as our understanding of disease pathology and the effect of nutrients on immunity and inflammation increases.

Most clinical dietary therapy studies undertaken so far have focused on some form of dietary elimination. Scandinavian health farms have long promoted fasting and vegetarian diets for patients with rheumatic diseases.

In 1979 and 1983, Sköldstam et al. [1, 2] carried out two studies to verify whether diet therapy could alleviate disease activity and symptoms in patients with RA. In one study, 16 RA patients fasted for 7–10 days and followed a lactovegetarian diet for the subsequent 9 weeks. There was a significant improvement in both objective and subjective disease symptoms during the fasting period, followed by rapid deterioration when the patients began on the lactovegetarian diet.

In the second study, 20 patients with RA completed a 7- to 10-day fast, followed by 3 months on a vegan diet (a diet without meat, fish or dairy products). Physician’s general assessment revealed that 11 patients had undergone subjective improvement, seven were unchanged and two were worse after the study period than before. Nineteen patients had lost weight and no improvement was seen in objective variables like erythrocyte sedimentation rate (ESR) and C-reactive protein during the dietary period. However, 5 (25%) of the patients showed both objective and subjective improvement. Several patients complained about the diet and only two patients had continued with a strict vegetarian diet after the study period. This confirms that many patients experience difficulty in implementing strict dietary changes.

In 1983, Panush et al. [3] conducted a study of the then popular Dong diet (which eliminated dairy products, red meat, citrus fruits, tomatoes, alcohol and coffee). This was an elegantly performed clinical dietary study with a double-blind, placebo-controlled design. Twenty-six patients took part, 11 on the experimental diet and 15 on a control diet. Although there was no statistical difference between the experimental and placebo diet groups, two patients in the experimental group improved noticeably. One patient experienced disease exacerbation after eating dairy products and the other after eating meat, spices and alcoholic beverages.

In 1986, Darlington et al. [4] published the results of a single-blinded, placebo-controlled study of 6 weeks of dietary manipulation in 53 patients with RA. During the first week, the patients were only allowed to eat foods they were unlikely to be intolerant to. In the article, it is not stated which food items these were. Other food items were then reintroduced one at a time to see whether any symptoms were elicited by the dietary challenge. Foods producing symptoms were then excluded from the diet. Both objective and subjective variables improved significantly, and a subgroup of 33 patients were graded as good responders. However, the patients were only observed for 6 weeks, which is a weakness in a study undertaken on patients with a chronic disease.

In 1991, we published the results of a single-blinded controlled clinical trial testing the effect on disease activity in patients with RA of dietary elimination combined with the vegetarian diet traditionally practised on Scandinavian health farms [5]. Fifty-seven patients took part in the study, 27 in the diet group and 26 in the control group. The patients were followed for 13 months, making this by far the most comprehensive study undertaken with regard to dietary therapy in RA.

We found statistically significant improvement in both objective and subjective disease variables in the diet group compared with the control group. Twelve patients (44%) in the diet group were responders, according to the Paulus criteria, compared with 2 (8%) in the control group [6]. Ten patients (37%) in the diet group reported aggravation of symptoms after reintake of one or more food items. Eight of these belonged to the responder group.

After 2 yr, we conducted a follow-up study on the same patients and found that the responders had continued with the diet and still had a significant reduction in all clinical disease variables and ESR [7]. In this study, 13 patients (59%) in the diet group reported an increase in disease symptoms after intake of meat, and 10 patients (45%) after intake of sugar and coffee. Of the 10 responders examined in the follow-up study, eight reported an increase in disease symptoms after intake of different kinds of meat, and six after intake of coffee, sweets and refined sugar.

Fasting has been documented to have beneficial effects on both clinical and laboratory variables reflecting disease activity in RA [1, 5, 8]. It thus serves as a useful model for studying the biological changes associated with simultaneous improvement in disease activity. Previous studies in healthy subjects have revealed that fasting decreases mitogen- and antigen-induced lymphocyte proliferative responses [9], and suppresses interleukin-2 (IL-2) production [10]. We have recently shown that a 7 day fast in RA patients also decreases CD4+ lymphocyte activation and numbers, suggesting transient immunosuppression [11]. We also found an increase in IL-4 production from mitogen-stimulated peripheral blood cells. Thus, further studies should be carried out to clarify the immunomodulatory mechanism behind fasting.

Evidence suggesting that food allergy, defined as an immunological response to food antigens or to intestinal bacterial flora, might be involved in disease pathology in most patients with RA is weak. However, it is possible that an exogenous agent like a food antigen can initiate a pathological immune process in a genetically susceptible individual [12].

Food antigens, food antibodies and their complexes have been detected in the systemic circulation of healthy subjects [13, 14]. Animal models indicate that the gut is an important trigger of and pathway for the immune response. Encounters with complex proteins, like gluten and milk proteins, lead to either oral tolerance or sensitization and possible loss of self-tolerance to cross-reacting epitopes [15].

An association between a special food item and disease activity has been reported by patients with a variety of rheumatic diseases, such as palindromic rheumatism [16, 17], systemic lupus erythematosus [18, 19], Sjögren’s syndrome [20] and juvenile RA (JRA) [21, 22]. Case reports describing an association between diet and disease activity in RA include both seropositive and seronegative disease [23–25]. Although the extent of food allergy involvement is still not known, it has been suggested that between 5 and 30% of patients with RA may be affected [26, 27].

We found an increase in humoral response in all patients with RA, with a general increase in IgG, IgA and IgM antibodies to various food antigens, like gluten and milk proteins. However, the elevated concentrations of specific immunoglobolins could not be used to predict which food items would aggravate the disease symptoms [28].

Wheat and other rough grain products can elicit an allergic T-cell response through their lectin structures. Lectins are glycoprotein molecules that bind to carbohydrate-specific receptors on lymphocytes with high affinity and thus elicit a significant immune response. Lentils and grain products have a particularly high lectin content. Lectins are fairly heat resistant; for example, lentils have to be cooked for a long time to inactivate the lectins.

While the results of a questionnaire-based survey revealed that 37–43% of patients with rheumatic diseases experienced an increase in disease symptoms after intake of certain food items, no difference could be found between the various diseases [29]. This suggests that diet may influence the inflammatory process in general and is not a specific feature of RA.

One of the mechanisms involved may be the release or secretion of vasoactive amines (bioactive amines) like histamine and serotonin [30]. Several of the food items reported to cause disease aggravation have a high histamine content, like pork and beef sausage, meat, tomato and spinach. Since no immunological response to pork and other meat has been demonstrated, a pharmacological response would explain the often reported increase in symptoms resulting from these foods [31]. Other foods like shellfish, strawberries, chocolate and fish can cause a release of histamine.

Citrus fruits, which contain other vasoactive amines (octopamine and phenylephrine), are often said to aggravate symptoms [30]. Consumption of both coffee and alcohol has been shown to liberate adrenaline and/or noradrenaline, which suggests that they have a pharmacological effect [30, 32]. Consumption of alcohol can also result in the release of histamine, and certain red wines have in addition a high concentration of histamine, which may explain the frequently reported intolerance.

A pharmacological reaction would also explain why the patients reported immediate reactions to these food items, as opposed to the more delayed reactions to dairy products and gluten. This may mean that a different mechanism is involved in symptom aggravation. The reported aggravation of symptoms after intake of refined sugar and sweets in patients with RA may have a metabolic explanation, such as an increased concentration of blood glucose due to impaired glucose handling [33–35].

Gut involvement in the pathogenesis of rheumatic diseases was proposed by Rea Smith [36], who reported that surgical removal of intestinal segments with focal infection had a beneficial effect on disease activity. Monroe and Hall [37] reported differences in the stools of 142 patients with chronic arthritis as compared with controls. Månsson and Olhagen [38] found not only an abnormal faecal flora, with an increase inClostridium perfringens in patients with RA, systemic lupus erythematosus and psoriatic arthropathies compared with healthy controls, but also a higher level of alpha-antitoxin in the serum of these patients. Alpha-toxin (phospholipase-C) is produced by a special strain of C. perfringens often found in RA patients. Månsson and Olhagen [38] found a rise in alpha-antitoxin titre in 75% of the patients with RA in the study, but in none of the controls.

A significantly higher carriage rate of C. perfringens in patients with RA than in healthy controls has also been documented by Shinebaum et al.[39]. An altered intestinal bacterial flora has been reported in patients with seropositive erosive RA compared with patients with seronegative RA and controls [40]. An increased concentration of antibodies to Proteus has been described in patients with active RA [41, 42] and to Klebsiella in patients with ankylosing spondylitis [43]. Several of these reports have suggested that RA and ankylosing spondylitis could be mediated by cross-reactivity between self and bacterial antigens.

The intestinal bacterial flora is known to be affected by diet [44–46], and it has been suggested that a diet which could alter the intestinal flora might have an effect on disease activity. This theory was supported by the finding that changes in disease activity correlated with alterations in the intestinal flora measured in patients who switched from an omnivorous to a vegetarian diet [47]. The effects of the intake of functional foods (i.e. food as medicine; in this case, food which promotes the growth of health-promoting bacteria in the intestine or food items that contain natural healthy intestinal bacteria) should be an interesting field for further research.

Much interest has been taken in recent years in the immunomodulatory effects of polyunsaturated fatty acids (PUFAs) and their therapeutic potential as anti-inflammatory agents [48]. Both clinical and in vitrostudies have established that long-chain n-3 and n-6 fatty acids inhibit T-lymphocyte function [49–52].

Research suggests that manipulating the balance of dietary fatty acids in favour of increased n-3 fatty acids and decreased n-6 fatty acids may have a beneficial effect on disease activity in RA [49, 53–56]. These studies have shown that long-chain n-3 fatty acids can diminish peripheral blood mononuclear cell proliferation and reduce the production of IL-1, IL-2, IL-6, tumour necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ). However, clinical studies on supplementation of ω-3 fatty acids have not supported the expectations raised by the laboratory findings [53–57].

The balance between unsaturated and saturated fatty acids may also affect lymphocyte proliferation (in vitro) [58]. The practical implications of these observations for the in vivo situation are currently unclear, but suggest that a diet which is high in unsaturated fatty acids and very low in saturated fatty acids may have a stronger immunosuppressive effect than that obtained by only n-3 fatty acid supplementation.

In this respect, the Mediterranean diet, with a low content of red meat and a high content of olive oil, is of interest. Olive oil has been shown to reduce lymphocyte proliferation, natural killer cell activity, adhesion molecule expression on lymphocytes and the production of pro-inflammatory cytokines in animal models [59]. In an intervention study in which dietary saturated fatty acids were partly replaced by olive oil, mononuclear cell expression of ICAM-1 was found to be significantly reduced [60].

It has also been reported that a very low intake of saturated fats is beneficial in multiple sclerosis, where, as in RA, CD4+ lymphocytes are thought to play a pathogenic role [61]. It is thus worth investigating whether a diet low in saturated fats, with a high content of olive oil and with n-3 supplementation, could have immunosuppressive effects in vivoand could thus be of benefit in the treatment of RA.

The pathological hallmark of RA is persistent destructive inflammation in the synovial membranes of joints, which leads to a gradual destruction of the supporting structures of the joints, such as bone and cartilage. Although the aetiology is still unknown, the inflammation resulting from the immunological reaction is quite well described. It is known that neutrophil granulocytes, macrophages and lymphocytes are activated, and that oxygen free radicals are produced [62]. Hence, a low concentration of antioxidants may perpetuate tissue destruction in RA. Free oxygen radicals and oxidative stress may also be of importance for the aetiology and chronicity of the inflammatory rheumatic diseases [63, 64]. Two epidemiological studies have recently suggested that antioxidants may play a protective role [65, 66].

The most important antioxidants known today are vitamin A, vitamin E, vitamin C, beta-carotene, the bioflavonoids, zinc and selenium. The antioxidant properties of vitamin A and vitamin E lead to a reduction in the oxidation catalysed by free radicals [67]. Vitamin E functions as a physiological antioxidant for the cell membrane and is the most important fat-soluble antioxidant in the cell membrane lipids [64, 68]. Zinc plays a significant role in antioxidant protection and immunity because it is a constituent of the cytoplasmic enzyme superoxide dismutase [69]. Selenium, on the other hand, is part of the glutathione peroxidase enzyme, which can react with peroxides formed during inflammation. Beta-carotene is a fat-soluble, chain-breaking antioxidant and a quencher of singlet oxygen, and is known, along with alpha-tocopherol, to be the most important element of the non-enzymatic antioxidant defence in biological systems [70, 71].

Low serum concentrations of selenium and zinc in RA patients were reported as early as 1978 [72] and were further investigated by Tarp et al.[73–75]. Mezes and Bartosiewicz [63] found reduced plasma vitamin A content in patients with RA. Honkanen et al. [76] found lower serum levels of vitamin A and E in patients than in healthy controls. Sklodowska et al.[64] found lower vitamin E concentrations in plasma in children with JRA than in controls. Studies have also shown reduced concentrations of zinc and selenium in children with JRA [77, 78].

The reduced serum concentrations of antioxidants found in patients with inflammatory rheumatic diseases do not appear to be a consequence of reduced dietary intake in these patient groups compared with healthy controls [78–80]. They may, therefore, indicate a high turnover of antioxidants and an increased antioxidant requirement in these patients which is necessary in order to balance the higher production of free radicals.

Although studies of supplementation with a single antioxidant have not shown disease reduction in RA patients, it is still possible that patients with an inflammatory rheumatic disease will benefit from supplementation with a combination of several antioxidants or from a dietary intake that exceeds the recommended dietary allowances.

Studies of immunomodulation have revealed that nutrients other than food proteins and fats also have an impact. The effects of fatty acids, antioxidants and food proteins on immunomodulation need to be investigated further, and so should the question of the involvement of the gut in the aetiology and pathology of rheumatic diseases. More knowledge on the effects of dietary components upon immunological function is necessary if the potential use of dietary therapy as a tool in the treatment of RA is to be adequately assessed.

Hello! the madness of the summer is over (which I thoroughly enjoyed!) and at last I manage to blog about this amazing experience.

So in July, I attended the first UK retreat run by the Overcoming MS UK (OMS) organisation, (now a registered UK charity), who allowed me to go so that I can hopefully help them to run workshops etc in the UK, to help people with MS understand the effects of diet and lifestyle modification on MS.

From left to right, this is Linda Bloom, patron & founder of OMS UK, who has MS herself and is very well, Sandra Neate, Prof Jelinek’s wife, an emergency medicine consultant in Australia, Professor Jelinek, professor of emergency medicine and author & founder of Overcoming MS ( & very fit & well with MS), Gary McMahon , head of OMS UK, all round top bloke, with a business management background, but utterly committed to health, having helped his wife recover form serious illness using dietary & lifestyle measures, Dr Craig Hassed, an Australian GP and medical university lecturer, author & international speaker on mindfulness, and me.

What did I expect?

Well, I expected that I’d already know it all ( how arrogant!) …. I expected that I’d enjoy meeting the Professor and crew, but might shy away from too much socialising, not wanting to feel different as an MS nurse…. I expected I’d be bored in the evenings and took lots of work to do…. and that I might get a bit hungry on the fully vegan diet provided, and took a big loaf of bread for my bedroom… and I expected that 90% of the focus would be on diet & supplements, with a sliver of meditation thrown in for good measure….

What actually happened?

a) I didn’t know it all… & I’ll share my new understandings here, b) I enjoyed meeting every person on the retreat, was inspired by the company of so many intelligent, stimulating individuals and couples who dare to think differently and think for themselves, had a lot of fun, was never once bored, never did any work (!), and am actively staying in touch with the group via an email group because I want to! c) Was absolutely stuffed, because the food was tasty, vibrant, delicious and really ‘stuck to your ribs’. d) I got my focus back through meditation, and realised how powerful the effects of even a boring daily grind of meditation that you don’t even want to do can be !!

for this, it helped having a little cell, with no TV or internet connection….

So, first impressions happened the evening before the retreat, when I went out for a meal with the OMS staff/trainers. Firstly, the Professor is seriously fit and healthy looking, and runs or swims daily more than I do in a week ( if not 2), and comes across as genuinely lovely, thoughtful, intelligent, educated, and kind person. He is obviously ably supported by his wife Sandra, who shares his qualities, diet & lifestyle, and took on the sessions about the structure & role of different fats.

During the meal, in conversation, the Professor talked about how he would like to slow down his international work running the retreats ( he does already have his full time academic medical work), and I felt honoured to hear him relate this personal anecdote, with some emotion:

He said that he had recently experienced a relaxation of the drive to always be working to get his message out there, and that it had caused him to wonder and reflect. For some reason his age suddenly became very meaningful to him, but he couldn’t work out why — until he suddenly realised that he had now passed the age that his mother had been when she died, severely affected by MS (she took her own life). And so somehow, he had ‘made it’ , and proved to himself the value of the work he’s been doing all these years.

I’m not going to re-iterate all the points of the OMS approach here, as I’ve talked about it many times, and its all available for free on http://www.overcomingMS.org , there’s the books, and also a forum on the website where people can discuss points; I’m just going to go into some of the things I hadn’t quite nailed.

We sat in a circle around the outside of a large room, or on beanbags in the middle, and there were about 40 people. Most people had come with their partner, and some on their own. Teaching was very good quality, and we had lots of time to ask questions and discuss fine points.

Here’s the Prof teaching, and Linda in mid leap… she & Gary had organised and were running the show, she had her new baby in attendance, and during the week was constantly jumping up and physically running, fetching, carrying, leaping over boxes & beanbags, & looking radiant throughout.

Flax seed oil – in the most recent research carried out by OMS ,taking this trumped fish oil for having reduced disease activity. The best amount and way to take it is 2 dessert spoons drizzled over food ( or used to dip bread or in salad dressing) daily, and apparently, the best tasting is from http://www.flaxfarm.co.uk I just got some, and can confirm, it looks like sunshine and tastes… nutty but fine. Going to see if I can get a discount for Bedford MS Therapy Centre….

Meditation

I’m no stranger to meditiation, having taken it up in my 20s, however, life had started getting on top of me, and when I attended the retreat, I was pretty stressed.

I was taken aback by the serious focus on meditation – every day, we started and finished the session with a half hour mindfulness meditation, led by Craig Hassed. I also did some of my meditation again in my room on a morning. It was hard! It is hard! But it is real – it has real, measurable mental and physical health benefits, and it’s worth doing every single day. By the end of the week I felt that I had met my real self again, and I was OK. Meditation deserves a post of its own, which I’ll do some time, but for now, here’s some links to give a taste of the sort of thing we were doing. Scroll down to guided meditations, mindfulness meditation (1,2 or 3) with Craig Hassed.

At the MS Therapy Centre, we are trialling a new electrical treatment for pain, called APS Therapy (See previous issues for an explanation!)

Here’s a round-up of our results so far.Some people have completed a course of treatment, some are ongoing, and some have only just started and had a few sessions. We are working hard to make sure we collect better data in future so we can answer more questions. We used the ‘Visual analogue pain scale’ which measures pain out of 10, with 0 being ‘no pain’ and 10 being ‘the worst possible pain’

Neuropathic pain in limb: 7/10 down to pain free; complete pain relief which lasts 4-5 days, but appears to need long term treatment as comes back after this time.

Neuropathic pain in the feet and feeling ‘like walking on hot sand’, constant, 6-7/10 down to 3-4/10 in 3 weeks, hot sand feeling down to ‘not very often’ and improvement in blue-ish discolouration due to poor circulation..

Hip pain 6/10 constantly, complete relief since the first week, has not returned, and a decrease in neuropathic pain in the leg from 4/10 to 2/10 in 3 weeks.

Back pain, 8-9/10, worse on exercise, down to pain-free, 2-3/10 on exercise. Treated x 2 weekly for 6 weeks. Has not returned, 1 month after end of treatment. Leg pain, ‘pounding, throbbing’, 8/10, down to pain-free, has started to creep back since recent sensory relapse.

Long term shoulder pain, 2-7/10 to ‘much better’ but has since had to stop treatment for personal reasons.

Hip pain 10/10 plus, no benefit. This could be because there’s a serious problem that needs attending to underlying the pain, or because high doses of opiate painkillers make the treatment less effective. We’ll be helping this person get the right investigations and treatment, and maybe try again later.

Arm pain, possibly radiating from shoulder, no cause detected by GP, 2-3/10 with episodes of stabbing pain 5-6 x a week at 10/10; down to 1& half/10, no episodes of stabbing pain after 2 weeks of treatment

Headaches, constant, 7/10 down to pain-free, and back pain 7/10, down to 1/10, plus complete relief from insomnia.

Hip pain, 8&1/2 /10, very severe, ‘sickening’, no change, although improvements in sleep pattern. We are helping this person get investigations carried out.

Hip pain, 7/10, 8/10 when worst, down to 4/10 after 3 treatments, but also had deep physio manipulation prior to starting!

Severe muscle spasm and spasticity, no change after 12 weeks +

MS fatigue; no change

MS fatigue; no change

Headaches, 4-6/10, 9/10 when worst, 2-3 x a week, for most of life, worse since starting Rebif, down to pain-free; has had one headache since starting therapy, when had not drunk enough water. Has not taken regular painkillers for weeks. Back pain, 4-6/10, 7-8/10 when bad, down to 3/10. Stopped Naproxen and Co-codamol use. Knee pain (which was unreported, as forgot about it) has disappeared. Much more energy, staying up past bedtime, cleaning.

Tennis elbow, 8/10, worst 10/10, now 6/10, worst 8/10, significantly improved range of motion and no sleep disturbance due to pain, after one week’s treatment ( and also carrying on with Bowen treatment)

So in summary, in our study so far, 18 people have used the APS Therapy at the Centre, 17 with MS and one member of staff. 2 tried APS for fatigue, and 1 for spasticity, and disappointingly, these conditions have not experienced a significant benefit to date.

15 people used APS Therapy for pain. Of these, 13 have felt a significant reduction in pain, and 2 have not. 2 also report a significant increase in energy. Of the people with pain, 5 have achieved pain-free. Of these, 2 people’s pain has not come back since completing the course, one needs to maintain therapy once a week, and 2 are still completing their course of treatment.

We’re delighted that Denise, who many of you will know already from the Gym, has now been employed 3 days a week to also help run this project and help people to use the APS machines at the Beds and Northants MS Therapy Centre. If you are having a problem with pain, you can come and see me (Miranda) for a full pain assessment. If APS Therapy seems like an appropriate course of action and you:

I will refer you on to Denise, to start a 6 week treatment plan. For some pain, APS Therapy may be able to completely and permanently resolve the problem. For some people it may not help at all, and for others, it may significantly reduce or resolve the pain, but need to be continued to keep getting the effect. In those cases we can help you to purchase your own machine direct from the manufacturers if you wish, and also to apply for charitable funding if money is a problem.

It’s very exciting to be working with such a new, drug-free treatment. We intend to start helping people to review their medication once they get a good result, with a view to reducing pain medication.

In 2012 an Australian research team led by Professor George Jelinek (Founder of Overcoming MS, http://www.overcomingms.org) published research in Neurological Sciences, a major international neurology journal, looking at the health related quality of life outcomes at 1 and 5 years after an intensive MS lifestyle intervention. The evidence presented showed an average of 20% improvement on MS quality of life scores across physical, mental and emotional domains for people with MS following a preventive risk factor modification approach to MS over a 5-year period.

Additionally, Professor Jelinekʼs team has also commenced a major international study of PwMS looking at the various factors in their diets and lifestyles, and their disease activity and disability. This will produce strong evidence about the effect of these factors in MS disease activity and progression. The respondents represent the widest possible range of ages, geographical regions, and with different types of MS. The outcomes of this research will be published in a series of papers during 2013 and Prof. Jelinek will discuss these findings at this seminar.

This presentation will be held on Thursday 4th July 2013 at The Belmont Hotel, De Montfort Street, Leicester, UK.